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At least 1,099 records · Page 61Linked to original sources
PubMed1994

Identification of the sex of human preimplantation embryos in two hours using an improved spreading method and fluorescent in-situ hybridization (FISH) using directly labelled probes.

Dual fluorescent in-situ hybridization (FISH) using X and Y chromosome specific probes has been used to identify the sex of human embryos for preimplantation diagnosis of X-linked disease. With a modified spreading method and directly labelled fluorescent DNA probes, we have examined the possibility of reducing the time of the FISH procedure from 7 to 2 h. A total of 17 normally fertilized human embryos were disaggregated and 98 intact blastomeres obtained. The spreading efficiency was 96% and FISH signals were obtained from 97% of nuclei. In all cases, sibling blastomeres from the same embryo were the same sex. Mosaicism was observed in some embryos. Five cells which lysed during the disaggregation process were spread to determine whether FISH was possible in these cells, but in all cases the morphology of the nuclei was poor and multiple signals were observed so that reliable diagnosis of sex was not possible. The data reported here confirm that by using an improved spreading method in combination with directly labelled DNA probes, we have increased the efficiency and reduced the time required for sexing embryos for preimplantation diagnosis of X-linked disease.

Blastomeres↗
PubMed1997

Concurrent partnerships and the spread of HIV.

OBJECTIVE: To examine how concurrent partnerships amplify the rate of HIV spread, using methods that can be supported by feasible data collection. METHODS: A fully stochastic simulation is used to represent a population of individuals, the sexual partnerships that they form and dissolve over time, and the spread of an infectious disease. Sequential monogamy is compared with various levels of concurrency, holding all other features of the infection process constant. Effective summary measures of concurrency are developed that can be estimated on the basis of simple local network data. RESULTS: Concurrent partnerships exponentially increase the number of infected individuals and the growth rate of the epidemic during its initial phase. For example, when one-half of the partnerships in a population are concurrent, the size of the epidemic after 5 years is 10 times as large as under sequential monogamy. The primary cause of this amplification is the growth in the number of people connected in the network at any point in time: the size of the largest "component'. Concurrency increases the size of this component, and the result is that the infectious agent is no longer trapped in a monogamous partnership after transmission occurs, but can spread immediately beyond this partnership to infect others. The summary measure of concurrency developed here does a good job in predicting the size of the amplification effect, and may therefore be a useful and practical tool for evaluation and intervention at the beginning of an epidemic. CONCLUSION: Concurrent partnerships may be as important as multiple partners or cofactor infections in amplifying the spread of HIV. The public health implications are that data must be collected properly to measure the levels of concurrency in a population, and that messages promoting one partner at a time are as important as messages promoting fewer partners.

Computer Simulation↗
PubMed2000

Intraocular melanoma spread to regional lymph nodes: report of two cases.

PURPOSE: To report two cases of regional lymphatic spread of primary uveal melanoma. METHODS: The clinical records of two patients who underwent enucleation for uveal melanoma and later developed regional lymph node metastases were reviewed. One of the two eyes was initially treated with proton beam irradiation. Histologic sections of the enucleated eyes and excised lymph nodes were examined. RESULTS: The melanomas arose in the choroid and ciliary body of the two patients and spread to regional lymph nodes 2 years after enucleation. The choroidal melanoma recurred after irradiation, diffusely infiltrated the uveal tract, and extended into the conjunctiva via an emissary canal. The ciliary body melanoma spread through the trabecular meshwork to the conjunctiva. CONCLUSIONS: Choroidal and ciliary body melanoma may rarely exhibit regional lymph node metastasis. This mode of metastasis may occur after extraocular spread and invasion of conjunctival lymphatics.

Adult↗
PubMed1996

Anatomic distribution of metastases in the vertebral body and modes of hematogenous spread.

STUDY DESIGN: A retrospective review of the magnetic resonance spine examinations of 49 patients with metastatic bone disease to the spine was performed. OBJECTIVES: To determine whether the pattern of metastatic distribution in the spine correlates with the type of primary tumor and theoretical mode of hematogenous spread by arterial or venous routes. SUMMARY OF BACKGROUND DATA: In 1940, Batson theorized a venous plexus route by which tumors spread to the spine from pelvic tumors such as prostatic carcinoma. It this theory is true, the venous vascular anatomy of the spine would result in metastases being deposited in the central or posterior vertebral body, whereas arterial deposits would occur near the end-plates. METHODS: Each vertebral body was divided into 27 equal cells in the magnetic resonance images; the central and posterior cells in the midsagittal view were defined as central, and the other cells were defined as peripheral. The primary tumor was assigned to either the arterial or venous group based on Batson's proposed mode of spread. The average number of lesions per involved vertebral body in the central and peripheral regions was calculated. RESULTS: There was no statistically significant correlation between tumors with proposed arterial/venous routes of metastasis and central/peripheral location of metastatic deposits. CONCLUSION: The mechanism by which tumors spread to the vertebral body may not be via a pure arterial or venous route. Other mechanisms such as tissue specificity, cascade system, and closed loop circulation system may be involved.

Adolescent↗
PubMed2004

Can highly active antiretroviral therapy reduce the spread of HIV?: A study in a township of South Africa.

BACKGROUND: Calls have been made for the large-scale delivery of highly active antiretroviral therapy (HAART) to people infected with HIV in developing countries. If this is to be done, estimates of the number of people who currently require HAART in high HIV prevalence areas of sub-Saharan Africa are needed, and the impact of the widespread use of HAART on the transmission and, hence, spread of HIV must be assessed. OBJECTIVES: To estimate the proportion of people eligible for combination antiretroviral therapy and to evaluate the potential impact of providing HAART on the spread of HIV-1 under World Health Organization (WHO) guidelines in a South African township with a high prevalence of HIV-1. DESIGN: A community-based cross-sectional study in a township near Johannesburg, South Africa, of a random sample of approximately 1000 men and women aged 15 to 49 years. METHODS: Background characteristics and sexual behavior were recorded by questionnaire. Participants were tested for HIV-1, and their CD4 cell counts and plasma HIV-1 RNA loads were measured. The proportion of people whose CD4 cell count was less than 200 cells/mm and who would be eligible to receive HAART under WHO guidelines was estimated. The potential impact of antiretroviral drugs on the spread of HIV-1 in this setting was determined by estimating among the partnerships engaged in by HIV-1-positive individuals the proportion of spousal and nonspousal partnerships eligible to receive HAART and then by calculating the potential impact of HAART on the annual risk of HIV-1 transmission due to sexual contacts with HIV-1-infected persons. The results were compared with those obtained using United States Department of Health and Human Services (USDHHS) guidelines. RESULTS: The overall prevalence of HIV-1 infection was 21.8% (19.2%-24.6%), and of these people, 9.5% (6.1%-14.9%) or 2.1% (1.3%-3.3%) of all those aged 15 to 49 years would be eligible for HAART (ranges are 95% confidence limits). In each of the next 3 years 6.3% (4.6%-8.4%) of those currently infected with HIV-1 need to start HAART. Among the partnerships in which individuals were HIV-1-positive, only a small proportion of spousal partnerships (7.6% [3.4%-15.6%]) and nonspousal partnerships (5.7%, [3.0%-10.2%]) involved a partner with a CD4 cell count below 200 cells/mm and would have benefited from the reduction of transmission due to the decrease in plasma HIV-1 RNA load under HAART. Estimates of the impact of HAART on the annual risk of HIV-1 transmission show that this risk would be reduced by 11.9% (7.1%-17.0%). When using USDHHS guidelines, the proportion of HIV-1-positive individuals eligible for HAART reached 56.3% (49.1%-63.2%) and the impact of HAART on the annual risk of HIV-1 transmission reached 71.8% (64.5%-77.5%). CONCLUSIONS: The population impact of HAART on reducing sexual transmission of HIV-1 is likely to be small under WHO guidelines, and reducing the spread of HIV-1 will depend on further strengthening of conventional prevention efforts. A much higher impact of HAART is to be expected if USDHHS guidelines are used.

Adolescent↗
PubMed2003

Regional spread of nonneurogenic tumors to the skull base via the facial nerve.

OBJECTIVE: This study examined the clinical and pathologic features of regional spread of nonneurogenic neoplastic disease to the intratemporal segments of the facial nerve. STUDY DESIGN: Retrospective review.SETTING Three tertiary referral centers. PATIENTS: Six patients with neoplastic disease of nonneurogenic origin involving segments of the facial nerve within the temporal bone. INTERVENTIONS: All patients underwent surgery with curative intent. Five patients received adjuvant radiation, and two received adjuvant radiation and chemotherapy. MAIN OUTCOME MEASURES: Histopathology, site of primary tumor, intratemporal location of regional spread along the facial nerve, degree of facial paralysis, and presence of residual disease. RESULTS: Five cases of malignancy were reported: one case of parotid adenoid cystic carcinoma, one case of parotid mucoepidermoid carcinoma, two cases of squamous cell carcinoma of the skin, and one case of an unidentified carcinoma. Perineural spread was histologically found in all cases of malignant disease. In addition, one case of benign pleomorphic adenoma of the parotid gland that circumferentially involved an intratemporal segment of the facial nerve was reported. Facial paralysis was present in five of six (83%) of cases. Four patients had unresectable malignant disease, and two died despite multimodality therapy. CONCLUSIONS: The facial nerve provides a route for the spread of neoplastic disease into the temporal bone, and perineural invasion is an important mechanism of invasion and motility of malignant disease. Nonneurogenic intratemporal tumors of the facial nerve are a rare but significant cause of facial paralysis.

Adult↗
PubMed2002

Histologic-genetic mapping by allele-specific PCR reveals intraurothelial spread of p53 mutant tumor clones.

Common and clinically important features of urothelial carcinomas are multifocality and a high rate of recurrence. Molecular studies demonstrated that multifocal tumors are frequently composed of one tumor clone spreading throughout the urothelial tract. A combination of histologic and genetic mapping of cystectomy specimens from bladder cancer patients is a valuable tool to study bladder carcinogenesis and tumor cell spread by correlating urothelial morphologic features and defined genetic alterations. In the present study, the primary tumors of 14 cystectomy specimens were investigated for p53 protein overexpression by immunohistochemistry and p53 gene mutation by genomic sequencing. Seven tumors showed a strong nuclear staining for the p53 protein. In six of seven tumors, a p53 gene mutation was detected. Allele-specific PCR of defined p53 mutations was established in five of six cases with a p53 mutation. Subsequent screening of the entire urothelial lining of each cystectomy specimen by allele-specific PCR revealed p53-mutant cell clones in urothelial patches with carcinoma in situ and dysplasia, but also frequently in histomorphologically normal urothelium adjacent to the tumor. The pattern of tumor cell spread indicated a continuous intraurothelial growth of the p53-mutant clone. P53 immunohistochemistry visually confirmed the presence of mutant cells in most of these samples. We conclude that allele-specific PCR is a highly sensitive and reliable method for tracking specific p53 mutant clones in the urothelium. Moreover, the detection of p53-mutant cells in histologically normal or preneoplastic urothelial areas in four patients with invasive bladder cancer indicates an extensive intraurothelial tumor cell spread. The excellent correlation of immunohistochemically positive urothelial patches with the presence of a specific mutation highlights the biologic significance of p53-positive cells in the urothelium of tumor patients.

Aged↗
PubMed1986

On the spatial spread of rabies among foxes.

We present a simple model for the spatial spread of rabies among foxes and use it to quantify its progress in England if rabies were introduced. The model is based on the known ecology of fox behaviour and on the assumption that the main vector for the spread of the disease is the rabid fox. Known data and facts are used to determine real parameter values involved in the model. We calculate the speed of propagation of the epizootic front, the threshold for the existence of an epidemic, the period and distance apart of the subsequent cyclical epidemics which follow the main front, and finally we quantify a means for control of the spatial spread of the disease. By way of illustration we use the model to determine the progress of rabies up through the southern part of England if it were introduced near Southampton. Estimates for the current fox density in England were used in the simulations. These suggest that the disease would reach Manchester within about 3.5 years, moving at speeds as high as 100 km per year in the central region. The model further indicates that although it might seem that the disease had disappeared after the wave had passed it would reappear in the south of England after just over 6 years and at periodic times after that. We consider the possibility of stopping the spread of the disease by creating a rabies 'break' ahead of the front through vaccination to reduce the population to a level below the threshold for an epidemic to exist. Based on parameter values relevant to England, we estimate its minimum width to be about 15 km. The model suggests that vaccination has considerable advantages over severe culling.

Animals↗
PubMed2006

Modelling the initial spread of foot-and-mouth disease through animal movements.

Livestock movements in Great Britain (GB) are well recorded and are a unique record of the network of connections among livestock-holding locations. These connections can be critical for disease spread, as in the 2001 epidemic of foot-and-mouth disease (FMD) in the UK. Here, the movement data are used to construct an individual-farm-based model of the initial spread of FMD in GB and determine the susceptibility of the GB livestock industry to future outbreaks under the current legislative requirements. Transmission through movements is modelled, with additional local spread unrelated to the known movements. Simulations show that movements can result in a large nationwide epidemic, but only if cattle are heavily involved, or the epidemic occurs in late summer or early autumn. Inclusion of random local spread can considerably increase epidemic size, but has only a small impact on the spatial extent of the disease. There is a geographical bias in the epidemic size reached, with larger epidemics originating in Scotland and the north of England than elsewhere.

Animals↗
PubMed1984

Pathogenesis of zosteriform spread of herpes simplex virus in the mouse.

Zosteriform spread of herpes simplex virus (HSV) infection occurs after primary inoculation of the skin of both outbred and inbred mice. With HSV type 1 strain SC16 few outbred animals died if they were inoculated when 8 weeks old whereas up to 50% of animals died if inoculated when 4 weeks old. However, at either age, zosteriform spread of infection occurred in almost all animals as it did when 4-week-old outbred animals were inoculated with the avirulent strain KOS. Thus, control of zosteriform spread must act by different mechanisms from those controlling the encephalitis which leads to death. During replication in the epidermis virus enters axons and could first be found in sensory ganglia 2 days after inoculation of the skin. Thereafter, it was found in the nerve roots and in skin within the same dermatome but remote from the site of inoculation. When sensory nerves to this latter area were cut during the 4 days after primary inoculation lesions developing as a result of zosteriform spread were either completely inhibited or, with later section, decreased in incidence. Mortality was not affected by such nerve section. Latent infection must be established in neurons serving areas of skin remote from the inoculation site since with HSV-1 strain SC16, recrudescent lesions on the pinna could be induced by stripping the skin of the ear when the original inoculation had been in the skin of the neck. Such recrudescent disease was not demonstrated in animals infected with HSV-1 strain KOS even though this virus efficiently established latent infection in sensory ganglia.

Acute Disease↗
PubMed2004

Polarized glycoprotein targeting affects the spread of measles virus in vitro and in vivo.

We have shown previously that basolateral targeting of plasmid-encoded measles virus (MV) F and H protein is dependent on single tyrosine residues in the cytoplasmic tails of the glycoproteins and is essential for fusion activity in polarized epithelial cells. Here, we present data on the functional importance of polarized glycoprotein expression for the cytopathic properties of infectious MV in culture and for pathogenesis in vivo. By the introduction of single point mutations, we generated recombinant viruses in which the basolateral targeting signal of either one or both glycoproteins was destroyed (tyrosine mutants). As a consequence, the mutated glycoproteins were predominantly expressed on the apical membrane of polarized Madin-Darby canine kidney cells. In contrast to parental MV, none of these virus mutants was able to spread by syncytia formation in polarized cells showing that the presence of both MV glycoproteins at the basolateral cell surface is required for cell-to-cell fusion in vitro. Using cotton rats as an animal model that allows MV replication in the respiratory tract, we showed that basolateral glycoprotein targeting is also of importance for the spread of infection in vivo. Whereas parental MV was able to spread laterally within the respiratory epithelium and from there to cells in the underlying tissue, tyrosine mutants infected only single epithelial and very few subepithelial cells. These data strongly suggest that basolateral targeting of MV glycoproteins helps to overcome the epithelial barrier and thereby facilitates the systemic spread of MV infection in vivo.

Amino Acid Sequence↗
PubMed1998

Dispersed repetitive DNA has spread to new genomes since polyploid formation in cotton.

Polyploid formation has played a major role in the evolution of many plant and animal genomes; however, surprisingly little is known regarding the subsequent evolution of DNA sequences that become newly united in a common nucleus. Of particular interest is the repetitive DNA fraction, which accounts for most nuclear DNA in higher plants and animals and which can be remarkably different, even in closely related taxa. In one recently formed polyploid, cotton (Gossypium barbadense L.; AD genome), 83 non-cross-hybridizing DNA clones contain dispersed repeats that are estimated to comprise about 24% of the nuclear DNA. Among these, 64 (77%) are largely restricted to diploid taxa containing the larger A genome and collectively account for about half of the difference in DNA content between Old World (A) and New World (D) diploid ancestors of cultivated AD tetraploid cotton. In tetraploid cotton, FISH analysis showed that some A-genome dispersed repeats appear to have spread to D-genome chromosomes. Such spread may also account for the finding that one, and only one, D-genome diploid cotton, Gossypium gossypioides, contains moderate levels of (otherwise) A-genome-specific repeats in addition to normal levels of D-genome repeats. The discovery of A-genome repeats in G. gossypioides adds genome-wide support to a suggestion previously based on evidence from only a single genetic locus that this species may be either the closest living descendant of the New World cotton ancestor, or an adulterated relic of polyploid formation. Spread of dispersed repeats in the early stages of polyploid formation may provide a tag to identify diploid progenitors of a polyploid. Although most repetitive clones do not correspond to known DNA sequences, 4 correspond to known transposons, most contain internal subrepeats, and at least 12 (including 2 of the possible transposons) hybridize to mRNAs expressed at readily discernible levels in cotton seedlings, implicating transposition as one possible mechanism of spread. Integration of molecular, phylogenetic, and cytogenetic analysis of dispersed repetitive DNA may shed new light on evolution of other polyploid genomes, as well as providing valuable landmarks for many aspects of genome analysis.

Amino Acid Sequence↗
PubMed1999

Organization of cyanobiphenyl liquid crystal molecules in prewetting films spreading on silicon wafers.

We observe prewetting films of 8CB (4'-n-octyl-4-cyanobiphenyl) spreading at room temperature on silicon wafers by ellipsometry and x-ray reflectivity. Ellipsometry indicates the formation of a nondense monolayer spreading in front of a 45-A-thick film. X-ray reflectivity, performed using a ribbon geometry for the liquid crystal (LC) reservoir, allows us to determine the organization of the 8CB molecules in the homogenous film. It consists of a trilayer stacking with a smecticlike bilayer standing above a polar monolayer with tilted molecules. We show that the thickness of the bilayer is equal to the smectic periodicity in the bulk material and that the tilt angle of the molecules in contact with the solid surface is close to 60 degrees, in good agreement with second-harmonic generation studies reported by other groups. Such organization can be precisely determined using x-ray reflectivity because it induces a modulation of the electron density along the normal to the surface. Furthermore, a study of the ellispometric profile of a drop heated in the nematic phase, where we observe a complete spreading of the LC, shows the complex structuration of the LC close to the solid interface. In particular, the spreading behavior of the trilayer compared to the subsequent smecticlike bilayers indicates the existence of specific interaction between the trilayer and silicon wafer.

Journal Article↗
PubMed1999

Damage spreading transition in glasses: a probe for the ruggedness of the configurational landscape.

We consider damage spreading transitions in the framework of mode-coupling theory. This theory describes relaxation processes in glasses in the mean-field approximation which are known to be characterized by the presence of an exponentially large number of metastable states. For systems evolving under identical but arbitrarily correlated noises, we demonstrate that there exists a critical temperature T0 which separates two different dynamical regimes depending on whether damage spreads or not in the asymptotic long-time limit. This transition exists for generic noise correlations such that the zero damage solution is stable at high temperatures, being minimal for maximal noise correlations. Although this dynamical transition depends on the type of noise correlations, we show that the asymptotic damage has the good properties of a dynamical order parameter, such as (i) independence of the initial damage; (ii) independence of the class of initial condition; and (iii) stability of the transition in the presence of asymmetric interactions which violate detailed balance. For maximally correlated noises we suggest that damage spreading occurs due to the presence of a divergent number of saddle points (as well as metastable states) in the thermodynamic limit consequence of the ruggedness of the free-energy landscape which characterizes the glassy state. These results are then compared to extensive numerical simulations of a mean-field glass model (the Bernasconi model) with Monte Carlo heat-bath dynamics. The freedom of choosing arbitrary noise correlations for Langevin dynamics makes damage spreading an interesting tool to probe the ruggedness of the configurational landscape.

Journal Article↗
PubMed1999

Molecular dynamics of a liquid drop spreading in a corner formed by two planar substrates.

Molecular-dynamics simulations were used to investigate the spreading of nonvolatile liquid drops in a solid corner formed by two planar substrates. To understand the effect of the corner on the spreading, liquid drops in a corner with angles of 45 degrees, 90 degrees, and 135 degrees as well as on a flat substrate were examined. Both the solid substrate and the liquid drop were modeled using the Lennard-Jones interaction potential in the present study. Simulation results show that the mass center of the liquid molecules migrated towards the corner as time evolved and the spreading rate increased as the corner angle decreased. It is found that the variation of the mean spreading area with time can be described by a general relation of A(t) approximately t, which is in agreement with results obtained by other investigators. The distribution of liquid atoms per unit normalized corner degree shows a similar trend for different corner angles.

Journal Article↗
PubMed2000

Enhancement of epidemic spread by noise and stochastic resonance in spatial network models with viral dynamics.

We extend a previous dynamical viral network model to include stochastic effects. The dynamical equations for the viral and immune effector densities within a host population of size n are bilinear, and the noise is white, additive, and Gaussian. The individuals are connected with an n x n transmission matrix, with terms which decay exponentially with distance. In a single individual, for the range of noise parameters considered, it is found that increasing the amplitude of the noise tends to decrease the maximum mean virion level, and slightly accelerate its attainment. Two different spatial dynamical models are employed to ascertain the effects of environmental stochasticity on viral spread. In the first model transmission is unrestricted and there is no threshold within individuals. This model has the advantage that it can be analyzed using a Fokker-Planck approach. The noise is found both to synchronize and uniformize the trajectories of the viral levels across the population of infected individuals, and thus to promote the epidemic spread of the virus. Quantitative measures of the speed of spread and overall amplitude of the epidemic are obtained as functions of the noise and virulence parameters. The mean amplitude increases steadily without threshold effects for a fixed value of the virulence as the noise amplitude sigma is increased, and there is no evidence of a stochastic resonance. However, the speed of transmission, both with respect to its mean and variance, undergoes rapid increases as sigma changes by relatively small amounts. In the second, more realistic, model, there is a threshold for infection and an upper limit to the transmission rate. There may be no spread of infection at all in the absence of noise. With increasing noise level and a low threshold, the mean maximum virion level grows quickly and shows a broad-based stochastic resonance effect. When the threshold within individuals is increased, the mean population virion level increases only slowly as sigma increases, until a critical value is reached at which the mean infection level suddenly increases. Similar results are obtained when the parameters of the model are also randomized across the population. We conclude with a discussion and a description of a diffusion approximation for a model in which stochasticity arises through random contacts rather than fluctuation in ambient virion levels.

Epidemiologic Methods↗
PubMed2000

Dynamical self-affinity of damage spreading in surface growth models

The dynamical anisotropic scaling properties of the surface growth models are restudied by use of the damage spreading concept. For that the vertical damage spreading distance d( perpendicular) of a damaged column as well as the lateral damage spreading distance d(||) is introduced. The scaling Ansatze for &dmacr;( perpendicular)(d(||),t), D(||) identical with and D( perpendicular) identical with<&dmacr;( perpendicular)> are suggested. The critical property of the probability distribution P(d(||),t) for the survived damages is also suggested. The suggested scaling relations are tested by simulating various growth models with substrate dimension d=1. From these results it can be concluded that the critical property or dynamical self-affinity of a surface growth model can also be determined by investigating the damage spreading.

Journal Article↗
PubMed2000

Percolation with long-range correlations for epidemic spreading.

A percolation model with long-range correlations was introduced to investigate the phenomena of epidemic spreading by Monte Carlo simulations. The correlation exponent alpha and pathogenic ratio s correspond to different spreading methods and pathogenicity of variant epidemics. As the correlation changes from a weak one to a strong one, the patterns change from site percolation to Eden cluster when pathogenic ratio s=1, or Leath percolation cluster when s<1. Corresponding to change of patterns, the fractal dimension increases up to space dimension. The critical behavior in epidemic spreading has been examined based on the model. It is found that correlation has a great influence on the threshold of spreading percolation.

Disease Outbreaks↗